@article{9768eced5e4e4f52864bf5f673ea9c42,
title = "Salmonella biofilms program innate immunity for persistence in Caenorhabditis elegans",
abstract = "The adaptive in vivo mechanisms underlying the switch in Salmonella enterica lifestyles from the infectious form to a dormant form remain unknown. We employed Caenorhabditis elegans as a heterologous host to understand the temporal dynamics of Salmonella pathogenesis and to identify its lifestyle form in vivo. We discovered that Salmonella exists as sessile aggregates, or in vivo biofilms, in the persistently infected C. elegans gut. In the absence of in vivo biofilms, Salmonella killed the host more rapidly by actively inhibiting innate immune pathways. Regulatory crosstalk between two major Salmonella pathogenicity islands, SPI-1 and SPI-2, was responsible for biofilm-induced changes in host physiology during persistent infection. Thus, biofilm formation is a survival strategy in long-term infections, as prolonging host survival is beneficial for the parasitic lifestyle.",
keywords = "Biofilms, Carrier state, CsgD, Salmonella, SsrB",
author = "Desai, {Stuti K.} and Anup Padmanabhan and Sharvari Harshe and Ronen Zaidel-Bar and Kenney, {Linda J.}",
note = "Funding Information: ACKNOWLEDGMENTS. We thank our colleagues at the Mechanobiology Institute for the following: Danesha Suresh and Jason Lim from the R.Z.-B. laboratory for assistance with worm maintenance, Ong Hui Ting for help with image analysis, Ti Weng for providing anti–phospho-SEK-1 and anti–total SEK-1 antibodies, and Diego Piita de Araujo and Melanie Lee for scientific illustrations. We thank Alexander Westermann and J{\"o}rg Vogel (Institute for Molecular Infection Biology), for helping to troubleshoot RNA isolations from persistently infected worms. We are grateful to Michael Sheetz (Mechanobiology Institute), Stephen Lory (Harvard Medical School), and Lalita Ramakrishnan (University of Cambridge) for comments on the manuscript. We acknowledge the CGC, which is funded by the NIH Office of Research Infrastructure Programs (Grant P40 OD010440), for providing strain SS104. We thank Matt Chapman (University of Michigan) for the kind gift of anti-CsgA antibody and Aaron White (University of Saskatchewan) for anti-CsgD and anti–O-antigen antibodies. We acknowledge the A*STAR Microscopy Platform/Electron Microscopy for assistance in sample processing and TEM imaging in this study and David Liebl, Head of Electron Microscopy, for additional comments. This study was funded by Research Centre of Excellence in Mechanobiology, National University of Singapore, Ministry of Education, Singapore and Grants MOE2018-T2-1-038, NIHR21-AI123640, and VA 510 1 BX000372 (to L.J.K.). Publisher Copyright: {\textcopyright} 2019 National Academy of Sciences. All rights reserved.",
year = "2019",
month = jun,
day = "18",
doi = "10.1073/pnas.1822018116",
language = "English (US)",
volume = "116",
pages = "12462--12467",
journal = "Proceedings of the National Academy of Sciences of the United States of America",
issn = "0027-8424",
publisher = "National Academy of Sciences",
number = "25",
}